Administración crónica de cafeína evita la alteración de la glucosa postprandial en ratas / Chronic caffeine administration prevents postprandial glucose disturbance in rats

La administración crónica de cafeína evita la alteración de la glucosa postprandial en ratas. El aumento en el consumo de la cafeína alrededor del mundo no es discutible, es así como su investigación se ha vuelto extensa en sus diferentes campos. Objetivo. Analizar los efectos de la administración crónica de cafeína en ratas alimentadas con dieta de cafetería, a través de evaluar índices de consumo, antropométricos y bioquímicos. Materiales y métodos. La dieta de cafetería es un modelo dietético equivalente a las características de la dieta occidental típica que origina síndrome metabólico en humanos. En esta investigación se realizó la administración crónica vía intraperitoneal de cafeína por ocho semanas a ratas adultas macho Wistar alimentadas con dieta de cafetería. Dada la poca evidencia acerca de los efectos biológicos y comportamentales de la administración crónica de dicha sustancia frente a un modelo de dieta de cafetería se evaluaron parámetros de consumo, antropométricos y bioquímicos. Resultados. La dieta de cafetería ocasionó anomalías asociadas al síndrome metabólico; no obstante, la administración de cafeína en las ratas alimentadas con esa dieta resultó ser un factor protector en la glucosa postprandial, más no en la alteración de la tolerancia a la glucosa o perfil lipídico. Conclusiones. La cafeína permitió proteger los niveles de glucosa postprandial al término del experimento y un descenso en el peso corporal y consumo de alimento solo en la primera semana. Sin embargo, no se observaron mejoras significativas en el perfil de lípidos, adiposidad, tolerancia a la glucosa y glucosa plasmática(AU)

Chronic caffeine administration prevents postprandial glucose disturbance in rats. The increase in caffeine consumption is not debatable, this is how his research has become extensive in his different fields. Objective. To analyze the effects of chronic administration of caffeine in rats fed a cafeteria diet, by evaluating consumption, anthropometric and biochemical indices. Previous studies refer to administering caffeine in diets high in carbohydrates and / or in fat that induce obesity or symptoms of metabolic syndrome. Material and methods. The cafeteria diet is a dietary model equivalent to the characteristics of the typical western diet that causes metabolic syndrome in humans. In this research, chronic intraperitoneal administration of caffeine was performed for 8 weeks to adult male Wistar rats fed a cafeteria diet. Given the little evidence about the biological and behavioral effects of the chronic administration of this substance against a cafeteria diet model, consumption, anthropometric and biochemical parameters were evaluated. Results. After eight weeks it was found that the cafeteria diet given to the controls caused abnormalities associated with the metabolic syndrome; regarding the administration of caffeine in the rats fed this diet, the treatment turned out to be a protective factor in postprandial glucose, but not in the alteration of glucose tolerance or lipid profile. Conclusions. Caffeine allowed to protect postprandial glucose levels at the end of the experiment and a decrease in body weight and food consumption only in the first week. However, no significant improvements were seen in lipid profile, adiposity, glucose tolerance, and plasma glucose(AU)

Diagnostic Criteria for Metabolic Syndrome in Diet-Induced Rodent Models: A Systematic Review.

BACKGROUND: Thousands of publications in recent years have addressed the induction of metabolic syndrome (MetS) in rodents. However, the criteria and the reference values for diagnosing this disease have not been defined. OBJECTIVE: Our main objective was to carry out a systematic review to gather evidence about the criteria for biochemical and anthropometric parameters in which scientific studies have relied on to report that rats developed MetS from a previous dietary manipulation. METHODS: We compiled characteristics and findings of diet-induced MetS with high-fat, high-carbohydrate, high-fat/high-carbohydrates, and cafeteria diet from PubMed and Science Direct databases published in the last 5 years. RESULTS: The results on the principal determinants for the syndrome, published in the reviewed articles, were chosen to propose reference values in the rat models of food induction. CONCLUSION: The values obtained will serve as reference cut-of points in the development of the disease; in addition, the compilation of data will be useful in planning and executing research protocols in animal models.

Diagnóstico prenatal de esquizencefalia. Reporte de caso y revisión de la literatura / Prenatal diagnosis of schizencephaly. Case report and literature review

RESUMEN La esquizencefalia es una patología de etiología desconocida que se caracteriza ecográficamente por presentar hendiduras que comunican el espacio subaracnoideo con los ventrículos laterales. Desde la primera publicación en 1941, se describe dos tipos: la esquizencefalia tipo I (labio cerrado), en la cual los bordes de la hendidura (labios) entran en contacto; y la esquizencefalia tipo II (labio abierto), cuyos bordes (labios) están ampliamente separados por líquido cefalorraquídeo, que es de peor pronóstico y la única diagnosticable antenatalmente. Se presenta el caso de diagnóstico prenatal de un feto con hallazgos ultrasonográficos de esquizencefalia tipo 2.

ABSTRACT Schizencephaly is a pathology of unknown etiology characterized by clefts that communicate the subarachnoidal space with the lateral ventricles. Two types have been described since the first paper published in 1941: Type I schizencephaly (closedlip), where the edges of the cleft (lips) come into contact; Type II schizencephaly (openlip) presents cleft edges (lips) that are widely open and filled by cephalo-spinal fluid. The latter has a worse prognosis and may be diagnosed antenatally. We present the case of a fetus with prenatal ultrasonographic findings of Type 2 schizencephaly.

Clinical, histological and molecular characteristics of Mexican patients with Fabry disease and significant renal involvement.

BACKGROUND AND AIMS: Fabry's disease (FD) is an X-linked lysosomal disorder caused by a deficiency of the enzyme α-galactosidase A that produces accumulation of glycosphingolipids with clinical abnormalities of skin, eye, kidney, heart, brain, and peripheral nervous system. We undertook this study to describe the molecular characteristics of the first four Mexican patients with diagnosis of FD with significant renal involvement, correlating these molecular characteristics with clinical, pathological and biochemical findings. METHODS: Genomic DNA from Mexican nonrelated patients with presumptive diagnosis of FD was sequenced by polymerase chain reaction (PCR). DNA sequences were compared against sequences in world data bank gene for alpha-galactosidase A (α-GLA, ENSG00000102393) using the BLAST database. RESULTS: Three patients were confirmed as having FD by displaying mutations in the α-GLA gene. The mutations found are a substitution (p.L243 F) in patient 1, and a substitution (p.A156 V) in patient 3. These two mutations had been previously reported. The new mutation was in patient 2 who displayed a deletion (c.260delA) changing the open reading frame from codon 86 and a stop codon at the 105th residue of the protein, (instead of 429 AA). The fourth patient had lack of mutations in any of the seven exons of α-GLA or 25 base-pair flanking regions; had mild manifestations with kidney histopathological diagnosis of FD that gave us a final diagnosis of atypical phenotype of FD. CONCLUSIONS: Although the sample is small, it gives a first idea of the molecular and clinical heterogeneity of FD in a Mexican population.